Endogenous reduction of miR‐185 accelerates cardiac function recovery in mice following myocardial infarction via targeting of cathepsin K

Li, Chuanchang; Qiu, Xueting; Sun, Quan; Zhou, Jiahao; Yang, Huijun; Wu, Wan‐Zhou; He, Lingfang; Tang, Cui; Zhang, Guogang; Bai, Yongping

doi:10.1111/jcmm.14016

Cited by 32 publications

(34 citation statements)

References 39 publications

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“…35 In another study, miR-185 reduction regulates hypoxia-induced myocardial infarction by targeting cathepsin K (catK), and promotes angiogenesis, as well as accelerating cardiac function recovery in mice. 36 In the present report, the bioinformatics analysis revealed a potential target of miR-185-3p was CaSR and we further confirmed this association by using dual luciferase reporter assay by knockdown or overexpression of miR-185-3p. Additionally, Pearson correlation showed a negative correlation between miR-185-3p and CaSR, whereas positive regulation was revealed between circHIPK3 and CaSR.…”

Section: Discussionsupporting

confidence: 76%

Silencing of circHIPK3 Inhibits Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction by Sponging miR-185-3p

Xu¹,

Wang²,

Wang³

2020

DDDT

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Section: Discussionsupporting

confidence: 76%

Silencing of circHIPK3 Inhibits Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction by Sponging miR-185-3p

Xu¹,

Wang²,

Wang³

2020

DDDT

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“…Compared to the wild‐type mice, double deletion of miR‐133a‐1 and miR‐133a‐2 mice show a 2.5‐fold increase in cardiomyocyte proliferation in hearts with an elevated expression of α‐smooth muscle actin (α‐SMA), which is critical for fibroblasts differentiation to myofibroblasts . miR‐185‐5p dramatically expresses lower in hearts from mice following MI than that from normal mice, and miR‐185‐5p has been confirmed to inhibit cell proliferations, migrations and tube formations at cellular level . These observations have implicated the critical functions of miRNAs in cardiac fibrosis following MI.…”

Section: Introductionmentioning

confidence: 92%

“…16 miR-185-5p dramatically expresses lower in hearts from mice following MI than that from normal mice, and miR-185-5p has been confirmed to inhibit cell proliferations, migrations and tube formations at cellular level. 17 These observations have implicated the critical functions of miRNAs in cardiac fibrosis following MI.…”

mentioning

confidence: 97%

MiR‐590‐3p regulates proliferation, migration and collagen synthesis of cardiac fibroblast by targeting ZEB1

Yuan

Pan

Wen

et al. 2019

J Cellular Molecular Medi

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Previous studies have implicated the attractive and promising role of miR‐590‐3p to restore the cardiac function following myocardial infarction (MI). However, the molecular mechanisms for how miR‐590‐3p involves in cardiac fibrosis remain largely unexplored. Using human cardiac fibroblasts (HCFs) as the cellular model, luciferase report assay, mutation, EdU assay and transwell migration assay were applied to investigate the biological effects of miR‐590‐3p on the proliferation, differentiation, migration and collagen synthesis of cardiac fibroblasts. We found that miR‐590‐3p significantly suppressed cell proliferation and migration of HCFs. The mRNA and protein expression levels of α‐SMA, Col1A1 and Col3A were significantly decreased by miR‐590‐3p. Moreover, miR‐590‐3p directly targeted at the 3’UTR of ZEB1 to repress the translation of ZEB1. Interfering with the expression of ZEB1 significantly decreased the cell proliferation, migration activity, mRNA and protein expressions of α‐SMA, Col1A1 and Col3A. Furthermore, the expressions of miR‐590‐3p and ZEB1 were identified in infarct area of MI model in pigs. Collectively, miR‐590‐3p suppresses the cell proliferation, differentiation, migration and collagen synthesis of cardiac fibroblasts by targeting ZEB1. These works will provide useful biological information for future studies on potential roles of miR‐590‐3p as the therapeutic target to recover cardiac function following MI.

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“…The surgery of MI was operated by ligation of left anterior descending coronary artery (LADCA) as described previously. 18,19…”

Section: Myocardial Infarction (Mi)mentioning

confidence: 99%

Up‐regulation of paired‐related homeobox 2 promotes cardiac fibrosis in mice following myocardial infarction by targeting of Wnt5a

Bai

Tang

Shan

et al. 2019

J Cellular Molecular Medi

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Cardiac fibrosis is a key factor to determine the prognosis in patient with myocardial infarction (MI). The aim of this study is to investigate whether the transcriptional factor paired-related homeobox 2 (Prrx2) regulates Wnt5a gene expression and the role in myocardial fibrosis following MI. The MI surgery was performed by ligation of left anterior descending coronary artery. Cardiac remodelling was assessed by measuring interstitial fibrosis performed with Masson staining. Cell differentiation was examined by analysis the expression of alpha-smooth muscle actin (α-SMA). Both Prrx2 and Wnt5a gene expressions were up-regulated in mice following MI, accompanied with increased mRNA and protein levels of α-SMA, collagen I and collagen III, compared to mice with sham surgery. Adenovirus-mediated gene knock down of Prrx2 increased survival rate, alleviated cardiac fibrosis, decreased infarction sizes and improved cardiac functions in mice with MI. Importantly, inhibition of Prrx2 suppressed ischaemia-induced Wnt5a gene expression and Wnt5a signalling. In cultured cardiac fibroblasts, TGF-β increased gene expressions of Prrx2 and Wnt5a, and induced cell differentiations, which were abolished by gene silence of either Prrx2 or Wnt5a. S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section. How to cite this article: Bai W-W, Tang Z-Y, Shan T-C, et al. Up-regulation of paired-related homeobox 2 promotes cardiac fibrosis in mice following myocardial infarction by targeting of Wnt5a.

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Endogenous reduction of miR‐185 accelerates cardiac function recovery in mice following myocardial infarction via targeting of cathepsin K

Cited by 32 publications

References 39 publications

Silencing of circHIPK3 Inhibits Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction by Sponging miR-185-3p

Silencing of circHIPK3 Inhibits Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction by Sponging miR-185-3p

MiR‐590‐3p regulates proliferation, migration and collagen synthesis of cardiac fibroblast by targeting ZEB1

Up‐regulation of paired‐related homeobox 2 promotes cardiac fibrosis in mice following myocardial infarction by targeting of Wnt5a

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